Monkeypox: a new differential diagnosis when addressing genital ulcer disease.

We describe a case of genital ulcer and inguinal adenopathies that were attributable to monkeypox virus infection. We suggest clinicians adopt a low threshold for suspicion, particularly when evaluating genital ulcer disease.

Mercury exposure induces proinflammatory enzymes in vascular fibroblasts / La exposición a mercurio induce la expresión de enzimas pro-inflamatorias en fibroblastos vasculares

Introduction: Previous studies show that mercury exposure increases cardiovascular risk, although the underlying cellular mechanisms have still not been fully studied. The aim of this project is to study, in vascular fibroblasts (VF), the effect of HgCl2 exposure on the expression of enzymes involved in the synthesis of prostanoids and reactive oxygen species (ROS). These molecules have been shown to participate in the inflammatory response associated with cardiovascular diseases. Material and methods: Adventitial VF cultures of Sprague-Dawley rat aortas, shown to be α-actin negative by immunofluorescence, were exposed to HgCl2 (0.05-5μg/mL) for 48h. mRNA and protein levels of cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase 1 (mPGES-1), thromboxane A2 synthase (TXAS), NADPH oxidase 1 (NOX-1), and 4 (NOX-4) where analyzed using qRT-PCR and western blot, respectively. NOX activity was determined by chemiluminescence. Results: HgCl2 exposure increased COX-2, mPGES-1, TXAS, and NOX-1 expression and NOX activity, and decreased NOX-4 expression. The increase in NOX-1 and COX-2 expression was abolished by the treatment with inhibitors of COX-2 (10μM celecoxib) and NOX (300μM apocynin, 0.5μM ML-171). Conclusions: 1) HgCl2 increases the expression of pro-inflammatory enzymes involved in ROS and prostanoid synthesis in VF. 2) There is a reciprocal regulation between COX-2 and NOX-1 pathways. 3) These effects can contribute to explain the increase in cardiovascular risk associated to mercury (AU)

Introducción: Estudios previos muestran que la exposición a mercurio aumenta el riesgo cardiovascular, sin embargo, los mecanismos celulares subyacentes no han sido esclarecidos completamente. Nuestro objetivo es estudiar el efecto de la exposición a HgCl2 sobre la expresión de enzimas involucradas en la síntesis de prostanoides y especies reactivas de oxígeno (ROS) en fibroblastos vasculares (FV). Se ha demostrado la participación de estas moléculas en la respuesta inflamatoria asociada a enfermedades cardiovasculares. Métodos: FV de la adventicia de aorta de ratas Sprague-Dawley, caracterizados por inmunofluorescencia como negativos para α-actina, fueron estimulados con HgCl2 (0,05-5μg/ml) durante 48 horas. Se analizaron los niveles de ciclooxigenasa-2 (COX-2), prostaglandina E sintasa 1 microsomal (mPGES-1), tromboxano A2 sintasa (TXAS), NADPH oxidasa 1 (NOX-1) y 4 (NOX-4) mediante qRT-PCR y western blot, respectivamente. La actividad de NOX se determinó mediante quimioluminiscencia. Resultados: La exposición a HgCl2 aumentó la expresión de COX-2, mPGES-1, TXAS y NOX-1, disminuyendo la expresión de NOX-4. El tratamiento con inhibidores de COX-2 (10μM celecoxib) y NOX (300μM apocynin, 0.5μM ML-171) abolió el aumento de la expresión de NOX-1 y COX-2, respectivamente. Conclusiones: 1) HgCl2 aumenta la expresión de enzimas proinflamatorias implicadas en la síntesis de ROS y prostanoides en FV. 2) Hay una regulación recíproca entre las vías de COX-2 y NOX-1. 3) Estos efectos pueden contribuir a explicar el aumento del riesgo cardiovascular asociado a la exposición al mercurio (AU)

Mercury exposure induces proinflammatory enzymes in vascular fibroblasts.

INTRODUCTION: Previous studies show that mercury exposure increases cardiovascular risk, although the underlying cellular mechanisms have still not been fully studied. The aim of this project is to study, in vascular fibroblasts (VF), the effect of HgCl2 exposure on the expression of enzymes involved in the synthesis of prostanoids and reactive oxygen species (ROS). These molecules have been shown to participate in the inflammatory response associated with cardiovascular diseases. MATERIAL AND METHODS: Adventitial VF cultures of Sprague-Dawley rat aortas, shown to be α-actin negative by immunofluorescence, were exposed to HgCl2 (0.05-5µg/mL) for 48h. mRNA and protein levels of cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase 1 (mPGES-1), thromboxane A2 synthase (TXAS), NADPH oxidase 1 (NOX-1), and 4 (NOX-4) where analyzed using qRT-PCR and western blot, respectively. NOX activity was determined by chemiluminescence. RESULTS: HgCl2 exposure increased COX-2, mPGES-1, TXAS, and NOX-1 expression and NOX activity, and decreased NOX-4 expression. The increase in NOX-1 and COX-2 expression was abolished by the treatment with inhibitors of COX-2 (10µM celecoxib) and NOX (300µM apocynin, 0.5µM ML-171). CONCLUSIONS: 1) HgCl2 increases the expression of pro-inflammatory enzymes involved in ROS and prostanoid synthesis in VF. 2) There is a reciprocal regulation between COX-2 and NOX-1 pathways. 3) These effects can contribute to explain the increase in cardiovascular risk associated to mercury.